The effect of beta-adrenergic receptor blockade on exercise-induced lipid peroxidation in man has been examined by measuring the production of pentane in expired air. For this purpose, five healthy male subjects were subjected to dynamic exercise of graded intensity on a cycle ergometer (10 min at 45%, 5 min at 60% and 75% maximal oxygen uptake 1 h after ingestion of either a placebo or 40-mg propranolol. At rest, mean pentane concentration [( pent]) with placebo was 4.13 pmol.l-1, SD 2.14. After exercise, this value significantly increased by 310% (17.1 pmol.l-1, SD 7.73, P less than 0.01). Oral administration of 40-mg propranolol significantly lowered the mean resting [pent] to 1.75 pmol.l-1, SD 0.77, P less than 0.05. After exercise, the increase of [pent] was much smaller (240%) and was less significant (P less than 0.2) than with the placebo. The mechanism of this inhibitory effect of propranolol remains to be elucidated. However, as indicated by the measurement of plasma myeloperoxidase concentration, it can be concluded that the antioxidant property of propranolol cannot be attributed to the inhibition of neutrophil activation, a possible source of free radicals during exercise.
This study addresses the question of whether tocopherol mobilization during exercise could be explained by a lipolysis effect. Nine healthy male subjects were submitted to dynamic exercise of graded intensity (45, 60, 75% VO2max) on a cycle ergometer after ingestion of either a placebo or 40 mg propranolol as beta-blocker. Plasma tocopherol concentration increased toward a peak value reached during or at the end of exercise. The magnitude of this increase did not differ in the two experimental conditions while plasma free fatty acids concentration was lowered under beta-adrenergic blockade by propranolol. From these results, we conclude that tocopherol mobilization during dynamic exercise does not depend on lipolysis.
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